Renal autoregulation of arterial blood pressure requires maintenance of plasma and extracellular fluid volumes. Two mechanisms are thought to be involved in renal autoregulation: the tubuloglomerular feedback (TGF) and a vascular myogenic mechanism. The objective of this project has been to characterize the nonlinear dynamics and the interactions of these autoregulation mechanisms by using induced broadband perturbations of arterial blood pressure and analyzing the resulting blood flow data with nonlinear modeling methodologies. Using the novel methodologies developed in Core Project #1, we were able to quantify the nonlinear dynamics and the interactions between the two regulatory mechanisms (myogenic and TGF). Comparisons of nonlinear models of renal blood pressure and flow data obtained for normotensive rats and spontaneously hypertensive rats show unambiguously that the relative effect of the TGF mechanism is diminished in hypertensive rats and for high-level of forcing. This finding advances our understanding of hypertension and may lead to more effective clinical treatments.